ArticleTumour virus research2025
Fibroblasts regulate the transcriptional signature of human papillomavirus-positive keratinocytes.
Article in Tumour virus research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- NFX1-123 is required for keratinocyte differentiation and HPV 16 DNA maintenance in early and persistent infection models.Journal of virology · 2026Article
- The utility of fibroblast co-culture for the maintenance of episomes in human papillomavirus-associated cancer models.mSphere · 2026Article
- Metabolic reprogramming of cholesterol biosynthesis drives macrophage-mediated immune suppression in HPV-negative cervical adenocarcinoma.Frontiers in immunology · 2026Article
- Multi-omics analysis unveils the role of cancer-associated fibroblasts in cutaneous squamous cell carcinoma.Cancer cell international · 2025Article
- The Utility of Fibroblast Co-culture for the Maintenance of Episomes in Human Papillomavirus-Associated Cancer Models.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
- Update of
Authors and funding
7 authors.
Funding
Abstract
Persistent human papillomavirus (HPV) infection is necessary but insufficient for viral oncogenesis. Additional contributing co-factors, such as immune evasion and viral integration have been implicated in HPV-induced cancer progression. It is widely accepted that HPV + keratinocytes require co-culture with fibroblasts to maintain viral DNA as episomes. How fibroblasts regulate viral episome maintenance is a critical knowledge gap. Here we present comprehensive RNA sequencing and proteomic analysis demonstrating that coculture with fibroblasts is supportive of the viral life cycle, and is confirmatory of previous observations. Novel observations suggest that errors in "cross-talk" between fibroblasts and infected keratinocytes may regulate HPV integration and drive oncogenic progression. Our co-culture models offer new insights into HPV-related transformation mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.